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Vijay Srinivasan

Publications and source records attributed to Vijay Srinivasan.

5 recordsLinked to original sources
PubMed2006

Spontaneous gasping decreases intracranial pressure and improves cerebral perfusion in a pig model of ventricular fibrillation.

INTRODUCTION: Spontaneous gasping is associated with increased survival in animal models of cardiac arrest and in observational studies of humans. The potential beneficial effect of gasping on cerebral perfusion may underlie the observed survival benefit, but mechanisms remain unknown. HYPOTHESIS: We hypothesized that spontaneous gasping in a pig model of ventricular fibrillation (VF) decreases intracranial pressure (ICP) and increases cerebral perfusion pressure (CePP) during VF in a pig model. METHODS: The 13 female farm pigs, weighing between 16 and 33 kg, were anesthetized with propofol and intubated, and then had VF induced for 8 min without intervention. Intrathoracic pressure (ITP), aortic pressure (AoP), and ICP were measured continuously. CePP and ITP were recorded simultaneously during three maximal gasps and correlated with gasping by Spearman rank correlation. RESULTS: Gasping during VF occurred in 13/13 pigs and followed a crescendo-decrescendo pattern. Each gasp was associated with a biphasic AoP (initial fall, then rise) and ICP (initial rise, then fall) morphology. Time to first gasp (r(2)=0.06), time to maximal gasp (r(2)=0.02), duration of gasping (r(2)=0.11) and frequency of gasping (r(2)=0.32) did not correlate significantly with CePP during gasping while depth of gasping exhibited a weak but significant correlation with CePP (r(2)=0.35, p=0.05). Maximal gasping occurred at 202+/-34 s from onset of VF and resulted in an average decrease in ICP from 27.4+/-5.8 to 20+/-6.7 mmHg, p<0.01 along with an increase in CePP from -0.05+/-10.9 to 11.5+/-12.6 mmHg, p<0.05. CONCLUSIONS: Spontaneous gasping during cardiac arrest decreased intra-cranial pressure and increased cerebral perfusion pressure significantly. These results may help explain why gasping is associated with improved cardiac arrest survival rates. Based upon this new understanding of the physiology of gasping, we speculate that investigation of devices that can enhance the physiological effects of gasping on intracranial pressure and cerebral perfusion should be prioritized.

Animals↗
PubMed2006

Rapid induction of cerebral hypothermia is enhanced with active compression-decompression plus inspiratory impedance threshold device cardiopulmonary resusitation in a porcine model of cardiac arrest.

OBJECTIVES: A rapid, ice-cold saline flush combined with active compression-decompression (ACD) plus an inspiratory impedance threshold device (ITD) cardiopulmonary resusitation (CPR) will cool brain tissue more effectively than with standard CPR (S-CPR) during cardiac arrest (CA). BACKGROUND: Early institution of hypothermia after CPR and return of spontaneous circulation improves survival and outcomes after CA in humans. METHODS: Ventricular fibrillation (VF) was induced for 8 min in anesthetized and tracheally intubated pigs. Pigs were randomized to receive either ACD + ITD CPR (n = 8) or S-CPR (n = 8). After 2 min of CPR, 30 ml/kg ice-cold saline (3 degrees C) was infused over the next 3 min of CPR via femoral vein followed by up to three defibrillation attempts (150 J, biphasic). If VF persisted, epinephrine (40 microg/kg) and vasopressin (0.3 U/kg) were administered followed by three additional defibrillation attempts. Hemodynamic variables and temperatures were continuously recorded. RESULTS: All ACD + ITD CPR pigs (8 of 8) survived (defined as 15 min of return of spontaneous circulation [ROSC]) versus 3 of 8 pigs with S-CPR (p < 0.05). In survivors, brain temperature (degrees C) measured at 2-cm depth in brain cortex 1 min after ROSC decreased from 37.6 +/- 0.2 to 35.8 +/- 0.3 in ACD + ITD CPR versus 37.8 +/- 0.2 to 37.3 +/- 0.3 in S-CPR (p < 0.005). Immediately before defibrillation: 1) right atrial systolic/diastolic pressures (mm Hg) were lower (85 +/- 19, 4 +/- 1) in ACD + ITD CPR than S-CPR pigs (141 +/- 12, 8 +/- 3, p < 0.01); and 2) coronary perfusion pressures (mm Hg) were higher in ACD + ITD CPR (28.3 +/- 2) than S-CPR pigs (17.4 +/- 3, p < 0.01). CONCLUSIONS: A rapid ice-cold saline infusion combined with ACD + ITD CPR during cardiac arrest induces cerebral hypothermia more rapidly immediately after ROSC than with S-CPR.

Animals↗
PubMed2004

An integrated digital microfluidic lab-on-a-chip for clinical diagnostics on human physiological fluids.

Clinical diagnostics is one of the most promising applications for microfluidic lab-on-a-chip systems, especially in a point-of-care setting. Conventional microfluidic devices are usually based on continuous-flow in microchannels, and offer little flexibility in terms of reconfigurability and scalability. Handling of real physiological samples has also been a major challenge in these devices. We present an alternative paradigm--a fully integrated and reconfigurable droplet-based "digital" microfluidic lab-on-a-chip for clinical diagnostics on human physiological fluids. The microdroplets, which act as solution-phase reaction chambers, are manipulated using the electrowetting effect. Reliable and repeatable high-speed transport of microdroplets of human whole blood, serum, plasma, urine, saliva, sweat and tear, is demonstrated to establish the basic compatibility of these physiological fluids with the electrowetting platform. We further performed a colorimetric enzymatic glucose assay on serum, plasma, urine, and saliva, to show the feasibility of performing bioassays on real samples in our system. The concentrations obtained compare well with those obtained using a reference method, except for urine, where there is a significant difference due to interference by uric acid. A lab-on-a-chip architecture, integrating previously developed digital microfluidic components, is proposed for integrated and automated analysis of multiple analytes on a monolithic device. The lab-on-a-chip integrates sample injection, on-chip reservoirs, droplet formation structures, fluidic pathways, mixing areas and optical detection sites, on the same substrate. The pipelined operation of two glucose assays is shown on a prototype digital microfluidic lab-on-chip, as a proof-of-concept.

Body Fluids↗
PubMed2004

Association of timing, duration, and intensity of hyperglycemia with intensive care unit mortality in critically ill children.

OBJECTIVE: To study the association of timing, duration, and intensity of hyperglycemia with pediatric intensive care unit (PICU) mortality in critically ill children. DESIGN: Retrospective cohort study. SETTING: PICU of a university-affiliated, tertiary care, children's hospital. PATIENTS: A total of 152 critically ill children receiving vasoactive infusions or mechanical ventilation. INTERVENTIONS: None. METHODS: With institutional review board approval, we reviewed a cohort of 179 consecutive children, 1 mo to 21 yrs of age, treated with mechanical ventilation or vasoactive infusions. We excluded 18 with <3 microg.kg(-1).min(-1) dopamine only, diabetes, or solid organ transplant and nine who died within 24 hrs of PICU admission. Peak blood glucose (BG) and time to peak BG during PICU admission, duration of hyperglycemia (percentage of PICU days with any BG of >126 mg/dL), and intensity of hyperglycemia (median BG during first 48 PICU hours) were analyzed for association with PICU mortality using chi-square, Student's t-test, and logistic regression. MEASUREMENTS AND MAIN RESULTS: Peak BG of >126 mg/dL occurred in 86% of patients. Compared with survivors, nonsurvivors had higher peak BG (311 +/- 115 vs. 205 +/- 80 mg/dL, p <.001). Median time to peak BG was similar in nonsurvivors (23.5 hrs; interquartile ratio, 5-236 hrs) and survivors (19 hrs; interquartile ratio, 6-113 hrs). Duration of hyperglycemia was longer in nonsurvivors (71% +/- 14% of PICU days) vs. survivors (37% +/- 5% of PICU days, p <.001). Nonsurvivors had more intense hyperglycemia during the first 48 hrs in the PICU (126 +/- 38 mg/dL) vs. survivors (116 +/- 34 mg/dL, p <.05). Univariate logistic regression analysis showed that peak BG and the duration and intensity of hyperglycemia were each associated with PICU mortality (p <.05). Multivariate modeling controlling for age and Pediatric Risk of Mortality scores showed independent association of peak BG and duration of hyperglycemia with PICU mortality (p <.05). CONCLUSIONS: Hyperglycemia is common in critically ill children. Peak BG and duration of hyperglycemia are independently associated with mortality in our PICU. A prospective, randomized trial of strict glycemic control in this subset of critically ill children who are at high risk of mortality is both warranted and feasible.

Adolescent↗